1. Field of the Invention
The present invention relates to exercise methods, and particularly to methods of reducing accumulation of lactic acid within an exercised muscle or joint, with attendant pain and stiffness.
2. Prior Art
An ever increasing preoccupation with physical fitness is generating continuous growth of the fitness industry and a steadily expanding variety of exercise methods and equipment. Such exercise methods and devices now provide focused development of each particular muscle group in both static and dynamic applications and all ranges of stress and resistance, from simple toning of muscle tissue to full body building objectives.
With respect to all of the various exercise forms, there is a general perception that muscular pain and stiffness are a natural and inherent aspect of exercise. The familiar adage, "No pain, no gain" suggests the tendency to measure the quality of a fitness program by the extent of pain which results. Although some muscle stiffness and pain are a necessary part of conditioning the body, the severity can be greatly reduced by dealing with the specific physiological aspects of exercise.
A muscle fiber, for example, contains two proteins, actin and myosin. These are present as threadlike structures. When these proteins combine to form actomyosin, the fiber is shortened or contracted to provide the primary muscle force response. The energy required for this chemical reaction is obtained from the conversion of adenosine triphosphate (ATP) to adenosine diphosphate (ADP). A nerve impulse arriving at a motor end-plate causes release of acetylchlorine, which initiates this conversion. A rapid breakdown of high-energy ATP into ADP and phosphorus results. The ADP must subsequently be converted back to the ATP to enable the cycle to continue.
The necessary energy is ultimately derived from the combustion of glucose with oxygen to form carbon dioxide. When oxygen is not immediately available in sufficient quantity, such as occurs in severe muscular exertion, a certain amount of energy is temporarily obtained from the conversion of glucose to lactic acid. This is enabled because the reaction does not require oxygen. Unfortunately, the accumulation of lactic acid in the muscle tissue causes it to tire more quickly, leading to termination of the exercise activity. Therefore, the energy derived from conversion of glucose to lactic acid is temporary, at best.
Some medical studies suggest, however, that lactic acidosis offers some benefit to a training program, provided certain physiological training factors are considered. For example, patients with certain lung diseases may experience improved training response with higher levels of blood lactate than where work rates elicit only low lactate levels. It is possible that lactic acidosis serves to facilitate oxyhemoglobin dissociation and O.sub.2 transport to the muscle cells. Obviously, these considerations may be interrelated. In summary, there are clearly opposing aspects of lactic acidosis which suggest both favorable and unfavorable effects, particularly where exercise programs are concerned.
From a layman point of view, lacticemia may simply be considered to be a build up of lactic acid in muscles and joints. This occurs when inadequate supplies of oxygen exist within the exercised tissue. The accumulation of lactic acid may result in pain, discomfort and muscle cramps. Obviously, the greater the stress and duration of exercise, the greater the likelihood of lacticemia.
Current methods of countering the effects of lactic acid include focusing on diet, massage and rest. A cool down period following exercise is the most common and probably the most effective prior art technique for reducing such post-exercise pain. This allows blood flow to sweep some of the accumulated lactic acid from the exerted area. Massage mechanically forces improved circulation and is very helpful in reducing pain and stiffness. Specialized diets can also assist in minimizing lactic acid formation.
Some exercise methods have been developed and encouraged as a means to minimize impact stress, such as is typically associated with exercise. U.S. Pat. Nos. 1,630,797; 4,109,905 and 4,577,859 teach improved in-place swimming methods to enable swimming in confined tanks or pools of limited dimension. U.S. Pat. Nos. 4,776,581; 4,875,673; 4,941,659; and 5,306,217 disclose other forms of aquatic exercise devices and methods that offer reduced stress. None of these patents, however, teach the need or suggest a solution for direct control of lacticemia.
What is needed, therefore, is an improved method of exercise that reduces the occurrence of lacticemia and thereby one of the primary causal factors of post-exercise pain and stiffness.